Q-omics provides the consensus-scored PTCD2 profile across patient tissues and cancer cell-line models. PTCD2 expression is associated with patient survival in 25 of 34 cancer types, with the highest sampling consensus in READ. Among the 18 cancer types available for tumor–normal comparison, PTCD2 is differentially expressed in 11, with the highest sampling consensus in THCA. Additionally, PTCD2 RNA expression shows 20,814 significant gene co-expression associations, with the highest sampling consensus in UVM. Together, these results highlight READ, THCA, and UVM as cancer lineages where PTCD2 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for PTCD2 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PTCD2 survival associations across molecular data types. PTCD2 RNA expression shows survival associations in the most cancer types (25), followed by mutation status (3) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PTCD2 RNA expression–survival associations across cancer types. High PTCD2 expression shows unfavorable associations in KICH, OV, UVM and CESC, but favorable associations in READ and KIRC. The READ Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p < 0.001). Together, the overview and detailed table identify READ as the clearest survival context for PTCD2 RNA expression.
This table summarizes PTCD2 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 11, while mass-spec protein shows differences in 3. The strongest signals are observed in THCA for RNA and CCRCC for protein.
This table ranks reproducible tumor–normal expression differences for PTCD2. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PTCD2 shows lower tumor expression in THCA and higher tumor expression in COAD, LUAD, CHOL, LUSC and LIHC. The THCA box plot shows higher PTCD2 RNA expression in normal versus tumor tissue (log2 FC = −0.818, t-test p < 0.001).
This table shows molecular features associated with PTCD2 in patient tissues and cancer cell lines. In patient samples, PTCD2 shows the broadest associations at the RNA and protein expression levels, with UVM recurring as the lineage with the largest associated feature set. In cancer cell lines, PTCD2 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in BREAST, while CRISPR and shRNA rows add functional-dependency signals in UPPER_AERODIGESTIVE_TRACT and LARGE_INTESTINE.
